Search PubMed⌕ Search

Biomedical subjects

K Kogure

Publications and source records attributed to K Kogure.

473 records · Page 27Linked to original sources
PubMedDate not supplied

Adrenergic control of cerebral blood flow and energy metabolism in the rat.

Studies in rats were designed to separate and define the roles of the intrinsic and extrinsic adrenergic neurons in the control of cerebral blood flow (CBF) and cerebral energy metabolism. The data suggest several conclusions: 1. Arterial sympathetic innervation plays a role in the autoregulation of cerebral circulation. 2. The central adrenergic neurons have several functions: a) they enhance cerebral vascular tone by action on alpha receptor sites. b) They play an important role in the metabolic control of CBF. The proton-sensitive receptor sites on blood vessel walls require beta-adrenergic input in order to function. c) They influence metabolic rate of brain tissue by acting on beta-receptor sites on the cell membrane.

Adrenergic Fibers↗
PubMedDate not supplied

The measurement of cerebral blood flow in the rat.

Cerebral blood flow (CBF) was determined in the rat under 70% nitrous oxide anesthesia and pentobarbital anesthesia. The application of the Fick principle technique of Kety et al. was modified utilizing 133Xe infused intravenously steadily for 30 seconds, at which time the animal was decapitated and the head frozen in liquid nitrogen. A prior femoral artery to femoral vein shunt was led through a polyethylene catheter of 0.13 ml volume. This catheter passed as a coil in a NaI crystal well-counter with the arterial 133Xe concentration curve recorded by a ratemeter-recorder system. The results of the hemispheric blood flow (HBF) were: under 70% nitrous oxide anesthesia in normocapnia (Paco2 38 mm Hg), 86 +/- 15 ml/100 gm per minute; with hypocapnia (Paco2 20 mm Hg), 40 +/- 5 ml/100 gm per minute; with hypercapnia (Paco2 63 mm Hg), 187 +/- 10 ml/100 gm per minute; and with pentobarbital anesthesia (Paco2 38 mm Hg), 41 +/- 8 ml/100 gm per minute.

Animals↗
PubMedDate not supplied

Protective effects of a novel calcium antagonist with platelet-activating factor-antagonistic action, F-0401, against ischemic brain damage.

The protective effects of a novel dihydropyridine calcium antagonist with platelet-activating factor-antagonistic action, F-0401, on ischemic brain damage were investigated using experimental ischemia models in rats and gerbils. F-0401 (1 and 10 mg/kg, i.p.) prevented increases in water content, determined by the wet-dry method, in ischemic areas 24 hr after 1 hr of middle cerebral artery occlusion in the rat. Pretreatment with F-0401 (1 and 10 mg/kg, i.p.) prevented extravasation of Evans blue dye in the brain following 2 hr of bilateral carotid artery occlusion and 2 hr of reperfusion in the rat. Pretreatment with F-0401 (1 and 10 mg/kg, i.p.) protected against neuronal damage to hippocampal CA1 pyramidal cells following 3 and 5 min of forebrain ischemia in the gerbil. Immunostaining against microtubule-associated protein-2 also demonstrated preservation of CA1 neurons in F-0401-treated animals. Thus, this study shows that F-0401 prevents the occurrence of brain edema, disruption of blood-brain barrier and neuronal damage caused by cerebral ischemia. The results demonstrate that F-0401 may be a powerful candidate as a therapeutic agent in the treatment of acute stroke in man.

Animals↗
PubMedDate not supplied

Effect of vinconate against alterations in [3H]naloxone, [3H]MK-801 and [3H]muscimol bindings after transient cerebral ischemia in gerbils.

We examined the alterations of opioid (naloxone), N-methyl-D-aspartate and gamma-aminobutyric acidA receptors in the gerbil brain 7 days after cerebral ischemia using [3H]naloxone, [3H]MK-801 and [3H]muscimol autoradiography, respectively. We also evaluated the effect of vinconate against the alterations in these receptors. Transient cerebral ischemia was induced for 10 minutes, and vinconate (100 and 300 mg/kg) was given intraperitoneally 10 minutes before ischemia. [3H]MK-801 binding showed a more severe reduction than [3H]naloxone binding 7 days after cerebral ischemia, whereas [3H]muscimol binding was unchanged in almost all brain regions. Vinconate showed a significant prevention against the reduction in [3H]naloxone binding in all brain areas. This drug also prevented a significant reduction in [3H]MK-801 binding in most of the brain regions. Furthermore, [3H]muscimol binding in vinconate-treated gerbils exhibited a significant increase compared with that in sham-operated animals. These results show that opioid and N-methyl-D-aspartate receptors are very sensitive to transient cerebral ischemia, whereas gamma-aminobutyric acidA receptors are particularly resistant. They also suggest that vinconate has a potent protective effect against the alterations of opioid and N-methyl-D-aspartate receptors. These findings might be of interest in relation to the mechanism of ischemic neuronal damage.

Animals↗